Alopecia & Vitiligo

HAIR TYPES Fetal hair - Adult hair - Lanugo hair : soft, fine, lightly pigmented hairs. Adult hair - Vellus hair : fine hairs cover most of the body of youngsters and adults. Terminal hair: long, coarse, pigmented hairs with larger diameters.

NUMBER OF HAIRS Scalp : about 1,00,000 hairs. Face : about 600 hairs /cm2. Rest of the body : about 60 hairs/cm2.

LENGTH, WIDTH AND GROWTH RATE Length : range from <1mm to > 1 meter. Average uncut scalp hair : 25 – 100 cm. Width : from 0.005 to 0.06mm. Growth rate: about 1 cm/ month (terminal hair).

FUNCTIONS 1. Protects body surface from external injury. 2. Helps in sensory function. Psycho – social importance. Forensic importance. i. Identification of race, sex, age and religion. ii. Cause of death- can be determined. iii. Time of death- can be determined. 5. Assist thermo- regulation: mainly in lower animals.

HAIR CYCLE It is believed that each hair follicle goes through 10-20 hair cycle in a life time. There are four phases- Anagen : growing phase. Catagen: involuting phase. Telogen : resting phase.

ANAGEN (GROWING PHASE) Last for about 1000 days. Follicular cells grow, divide and become keratinized to form growing phase. A darkly pigmented portion is evident just above the hair bulb.

CATAGEN Lasts for about 10 days. Scalp hairs show a gradual thinning and decrease of the pigment. Melanocytes cease producing melanin.

TELOGEN Lasts for about 100 days. Club-shaped proximal end shed from the follicle during telogen or subsequent anagen. Growth of a new anagen hair leads to shedding of any remaining telogen hair. But new hair does not “push out” the hair from the previous cycle.

Alopecia None Scaring (Reversible) Scaring (Irreversible) . X

Alopecia Areata

Sudden hair loss ( localized or generalized) Alopecia Areata affects up to 2% 75% : Self recovery, 2-6 m Causes : 30%: +ve Family history autoimmune

ALOPECIA AREATA . Etiology It is an autoimmune disease- Exact cause is still unknown. It is an autoimmune disease- - Modified by genetic factors

ALOPECIA AREATA . -Triggered by environmental factors- Trauma. Neurogenic inflammation. Infections agents.

ASSOCIATED DISEASE Higher incidence of alopecia areata in patients of- 1. Atopic dermatitis. 2. Autoimmune disease – * SLE * Thyroiditis. * Myasthenia gravis. * Vitiligo. 3. Lichen planus. 4. Down syndrome.

Clinical features Well demarcated Exclamation point Normal scalp Nail: pitting, ridges

CLINICAL FEATURE Rapid and complete loss of hair in one or several patches. Site – Scalp, bearded area, eyebrows, eye lashes and less commonly other areas of body. Size – Patches of 1-5 cm in diameter.

CLINICAL FEATURE “Exclamation point” hair- at the periphery of hair loss, there are broken hairs, whose distal ends are broader than the proximal end.

Types of alopecia areata - Localized partial - Localized extensive - Alopecia ophiasis - Alopecia totalis - Alopecia universalis

OPHIASIS PATERN OF ALOPECIA AREATA

ALOPECIA UNIVERSALIS

Diagnosis Clinically H/E: sworm bees

DIFFERENTIAL DIAGNOSIS 1. Tinea capitis. 2. Trichotilomania. 3. Secondary syphilis

Treatment 1. Observation 2. Intralesional Corticosteroids 3. Skin Sensitizers Anthraline Diphencyclopropenone (DPCP) others

Others Topical steroids Systemic Steroids Cytotoxic Rx Phototherapy Minoxidil Hair Transplant

TREATMENT Spontaneous recovery is extremely common for patchy alopecia areata. For localized patchy alopecia areata- • Steroid- both local (intralesional and topical) and systemic (in short course).

Bad prognostic factors Young age Atopy Alopecia totalis, universalis, ophiasis Nail changes

Androgenetic Alopecia (Male and Female Pattern Hair Loss)

ANDROGENETIC ALOPECIA Definition : It is a very common, potentially reversible scalp hair loss that generally spares parietal and occipital areas (Hippocratic wreath) of the scalp.

Androgen dependent loss of scalp hair Androgenetic Alopecia affects up to 50% of males and 40% of females Autosomal dominant with variable penetrance 85% : +ve family history

DihydorTestosterone (Active) Miniaturization of Terminal Hairs 5 ALPHA Reductase Testosterone DihydorTestosterone (Active) Miniaturization of Terminal Hairs

Male Pattern Hair Loss

PATTERN OF HAIR LOSS

Androgenetic alopecia in women Maintenance of frontal hair lines with only slight recession. Etiology : Genetic Predisposition, Androgen excess, Ovarian cause- - Polycystic ovarian syndrome, - Other ovarian tumor

Female Pattern Hair Loss

ANDROGENETIC ALOPECIA IN WOMEN

CLINICAL FEATURE Other evidence of androgen excess: Acne. Hirsutism. Menstrual irregularities.

Treatment Topical:Neoxidil 2%- 5% solution Systemic: Fenastride or Spironolactone Surgical treatment- Micrograft & minigraft from non-androgen dependent site (occiput).

TELOGEN EFFLUVIUM It is a reaction pattern to a variety of physical and mental stressors represents a precipitous shift of a percentage of anagen hairs to telogen.

Telogen effluvium Chronic alopecia Reversible (but may be become chronic) 3-4 months

Causes of Telogen Effluvium None specific Endocrine - Hypo or hyperthyroidism. - Postpartum. - Peri or postmenopausal state. Nutritional - Biotin deficiency. - Essential fatty acid deficiency. - Iron deficiency. - Protein deprivation. - Zinc deficiency.

Causes

Causes of Telogen Effluvium (Contd.) Drugs Angiotensin-converting enzyme inhibitors. Anticoagulants. Antimitotic agents. Benzimidazoles. Beta blockers. Interferon Lithium

Causes of Telogen Effluvium (Contd.) Oral contraceptives. Retinoids. Vitamin A excess. Physical stress Surgery. Systemic illness. Psychological stress

Pathology > 12% to 15% of terminal follicles are in telogen. Follicle itself is not diseased. No inflammation or dystrophic changes.

CLINICAL PRESENTATION Diffuse hair loss with clinically perceptible thinning of hairs usually 3-5 weeks of inciting signal and shedding continue for about 3-4 month after removal of inciting cause. 150 to > 400 hair loss daily. Hair density may take 6-12 months to return to base line. Pull test. Clip test.

TREATMENT No specific therapy. In majority cases hair will grow spontaneously within few month after removing inciting cause. In some patients with chronic telogen effluvium- - 5% minoxidil solution .

Anagen effluvium Always related cytotoxic chemotherapy Acute and severe alopecia Mostly reversible but not always

TRICHTILLOMANIA A neurotic practice of plucking or breaking hair from scalp or eyelash resulting usually localized or widespread areas of alopecia contains hairs of varying length. Mostly girls under age of 10 years. Disturbed mother- child relationship.

TRICHOTILOMANIA

Scaring Alopecia SLE—DLE LP Sarcoidosis Leprosy Kerion - Favus Trauma

Vitiligo -Acquired cut. depigmentation -Kobner phenomena Causes Genetic Autoimmune dis. Neural Natural coarse? Varied

Why? Loss of normal melanocytes Dopa stain

Special studies T4, TSH, FBS ANA/Ro/La (prior to PUVA)

TREATMENT Sunscreen (sunburn, koebnerization, tanning) Limited: Class 3 topical GC Topical Tacrolimus Topical PUVA Excimer laser Resistant, Stable of 2 years : Surgical Generalized Phototherapy Universal: Bleaching agent

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